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2.
Imeta ; 2(3): e125, 2023 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-38867928

RESUMO

Heart failure (HF) is a sophisticated syndrome with structural or functional impairment of ventricular filling or ejection of blood, either causing symptoms and signs or being asymptomatic. HF is a major global health issue affecting about 64.3 million people worldwide. The gut microbiota refers to the complex ecosystem of microorganisms, mainly bacteria, in the gut. Studies have revealed that the gut microbiota is associated with many diseases ranging from neurodegenerative diseases to inflammatory bowel disease and cardiovascular diseases. The gut hypothesis of HF suggests that low cardiac output and systemic circulation congestion would cause insufficient intestinal perfusion, leading to ischemia and intestinal barrier dysfunction. The resulting bacterial translocation would contribute to inflammation. Recent studies have refined the hypothesis that changes of metabolites in the gut microbiota have a close relationship with HF. Thus, the gut microbiota has emerged as a potential therapeutic target for HF due to both its critical role in regulating host physiology and metabolism and its pivotal role in the development of HF. This review article aims to provide an overview of the current understanding of the gut microbiota's involvement in HF, including the introduction of the gut hypothesis of HF, its association with HF progression, the potential mechanisms involved mediated by the gut microbiota metabolites, and the impact of various interventions on the gut microbiota, including dietary interventions, probiotic therapy, fecal microbiota transplantation, antibiotics, and so on. While the gut hypothesis of HF is refined with up-to-date knowledge and the gut microbiota presents a promising target for HF therapy, further research is still needed to further understand the underlying mechanisms between gut microbiota and HF, the efficacy of these interventions, and contribute to the health of HF patients.

3.
Front Immunol ; 13: 874932, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35860268

RESUMO

Immunotherapy utilizing programmed cell death-1 (PD-1)/PD-L1 inhibitors has been regarded as a rising hope for tumor patients, and their effects have been demonstrated in many clinical trials. However, immune-related adverse events also occur in patients and can sometimes have severe consequences. Pembrolizumab (Keytruda) is a humanized monoclonal anti-PD-1 antibody that has been approved by the US Food and Drug Administration for non-small-cell lung cancer. Here, we report a rare case of an abdominal fibroinflammatory reaction that affected multiple organs during anti-PD-1 immunotherapy using pembrolizumab in a non-small-cell lung cancer patient. The patient's case demonstrates that immunotherapy-related abdominal fibroinflammatory reactions need to be considered, especially for patients with a history of pre-existing conditions in the abdomen. Glucocorticoids may be useful as a treatment when a diagnosis is confirmed.


Assuntos
Carcinoma Pulmonar de Células não Pequenas , Neoplasias Pulmonares , Abdome , Apoptose , Antígeno B7-H1 , Carcinoma Pulmonar de Células não Pequenas/patologia , Humanos , Neoplasias Pulmonares/patologia
4.
Aging Dis ; 13(1): 144-156, 2022 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-35111367

RESUMO

Coronavirus disease 2019 (COVID-19) is still an ongoing pandemic worldwide. COVID-19 is an age-related disease with a higher risk of organ dysfunction and mortality in older adults. Coagulation disorders and thrombosis are important pathophysiological changes in COVID-19 infection. Up to 95% of COVID-19 patients have coagulation disorders characterized by an elevated D-dimer, a prolonged prothrombin time, a low platelet count and other laboratory abnormalities. Thrombosis is found in critical cases with an increased risk of death. Endothelial cells are prone to be affected by the novel SARS-CoV-2 and express angiotensin-converting enzyme 2. The evidence, such as the presence of the virus, has been identified, leading to the inflammation and dysfunction. Endothelial cell activation and dysfunction play a pivotal role in the hypercoagulation status in COVID-19 patients. In addition to the direct exposure of subendothelial tissue to blood, Weibel-Palade bodies within the endothelium containing coagulants can be released into the circulation. Endothelial nitric oxide synthase may be impaired, thus facilitating platelet adhesion. Moreover, anti-ß2-glycoprotein I antibodies may also contribute to the coagulopathy in COVID-19 by inducing the upregulation of proinflammatory mediators and adhesion molecules. To conclude, coagulation disorders and thrombosis are vital and predict a poor outcome in COVID-19 patients, especially in severe cases. Endothelial cell activation and dysfunction may play an important role in causing clot formation. More basic and clinical research is warranted to further our understanding of the role of coagulopathy and their possible mechanism in COVID-19 patients.

5.
Exp Ther Med ; 21(4): 404, 2021 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-33692835

RESUMO

Systemic mastocytosis (SM) is a heterogeneous disease of the bone marrow, which is characterized by the abnormal proliferation and infiltration of mast cells in one or more organs, such as the skin, bone marrow, digestive tract, liver and spleen. Urticaria pigmentosa is a typical but infrequent manifestation of SM. Other clinical presentations are non-specific, varying from pruritus and hypotension to multiple organ dysfunction, which may be lethal when hemodynamic changes occur, such as the sharp decline in blood pressure observed in the present case. In patients who lack skin lesions, the diagnosis of SM is frequently challenging. The present study reported on a 58-year-old male who presented with episodic flushing and syncope. The patient demonstrated marked neutrophilia and reduced blood potassium concentrations soon after the onset of each episode, which was able to last several hours, ranging from once to four times a year. SM without skin lesions was suspected and confirmed after multifocal bone marrow aspiration, which revealed dense infiltrates of mast cells (≥15 mast cells), with positive toluidine blue and CD117 staining. The present case illustrates the significance of taking SM or mast cell activation syndrome into consideration when unexplained recurrent hypotension or even syncope are observed, care should be taken to exclude differential diagnoses, as some of them may have much poorer prognoses and require alternative treatments.

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